Morton Ch40

Patient Management:Gastrointestinal SystemVALERIE K. SABOL ■ ALLISON G. STEELE

Enteral NutritionMethods of Enteral Nutrition

DeliveryTypes and Delivery of Enteral

FormulasComplications of Enteral Nutrition

Parenteral (Intravenous) NutritionMethods of Parenteral Nutrition

DeliveryComplications of Parenteral

NutritionTerminating Parenteral Nutrition

Role of the Nurse in NutritionalSupport

objectivesBased on the content in this chapter, the reader should be able to:■ Explain how physiological stresses of illness and injury alter the

body’s needs for energy.■ Identify and describe the different forms of malnutrition.■ Identify and describe enteral and parenteral nutrition with regard

to indications, assessment, management, and complications.

chapter

40

Health and nutrition have a symbiotic relationship.Physiological stressors, such as illness and injury,alter the body’s metabolic and energy demands.

Although early identification and nutritional interventioncan lessen morbidity and mortality risks in critically illpatients, it is often the underlying disease process that mustbe identified and corrected before the body can reverseabnormal nutrient metabolism.1,2 This chapter presents anoverview of physiological stress and its effect on metabo-lism, types of malnutrition, and the indications, assessment,and management of enteral and parenteral nutrition sup-port therapies and the complications associated with thesetherapies.

In addition to the variety of macronutrients and micro-nutrients that are discussed later in this chapter, it is impor-tant to understand the variety of medications administeredto the critically ill to combat disease processes and theirassociated side effects. Table 40-1 summarizes many of thecommon gastrointestinal medications administered to crit-ically ill patients who are concurrently receiving nutritionsupport therapy.

According to the laws of thermodynamics, energy canbe neither created nor destroyed. Through the processesof metabolism, people obtain energy from the foods (ororganic fuels) they consume. Metabolism has two parts:

anabolism and catabolism. Anabolism is a building-up andrepair process that requires energy. Catabolism consists ofbreaking down food and body tissues for the purpose ofliberating energy.

Glucose is the obligatory fuel of the body, and of thebrain and nervous system in particular. The nervous systemcannot store or synthesize glucose as a fuel source, so itrelies on glucose extraction from the bloodstream. Thebrain and nervous system depend on glucose to meet theirmetabolic requirements. The liver regulates glucose entryinto the circulatory system because it has the ability to bothstore and synthesize glucose. Excess glucose is convertedand stored as either glycogen or fatty acids (triglycerides).Although glucose can be converted to fatty acids for stor-age, there is no pathway for converting fatty acids back toglucose. Instead, fatty acids are used directly as a fuel sourceor are converted to ketones by the liver. After prolongedstarvation, the body adapts to preserve vital proteins byusing ketones, rather than glucose, as energy. Ketoacidosisoccurs when ketone production exceeds utilization.

The pancreatic hormones glucagon and insulin haveopposing functions in metabolic processes. Glucagonstimulates glycogenolysis (glycogen breakdown) and glu-coneogenesis (the process of glucose synthesis from other

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CHAPTER 40 Patient Management: Gastrointestinal System 3

table 40-1 ■ Mechanisms of Action, Indications, Common Adverse Effects, and Comments for Common Gastrointestinal Medications

Common Agent Mechanism of Action Indication Adverse Effects Comments

AntacidsAluminum carbonate

Aluminum hydroxide(Amphojel, AlternaGEL)

Calcium carbonate (Tums, Caltrate)

Magnesium hydroxide (Milk of Magnesia)

Dihydroxyaluminum, sodium carbonate (Rolaids)

Histamine Type 2 (H2) Receptor AntagonistsCimetidine (Tagamet)

Ranitidine (Zantac)

Famotidine (Pepcid)

Nizatidine (Axid)

Proton Pump InhibitorsOmeprazole (Prilosec),

lansoprazole (Prevacid),rapeprazole (Aciphex),pantoprazole (Protonix),esomeprazole (Nexium)

Neutralization of gastricacid; binding phos-phates in the gastro-intestinal tract

Neutralization of gastricacid; binding phos-phates in the gastro-intestinal tract

Neutralization of gastricacid

Neutralization of gastricacid

Neutralization of gastricacid; reduction ofpepsin

Inhibition of histamineat H2 receptor siteson gastric parietalcells, which inhibitsgastric acid secretion




Suppression of gastricacid secretion by inhi-bition of H+, K+-ATPasepump (proton pump)of parietal cells, block-ing final step in acidproduction

Symptomatic relief ofgastric irritation, pre-vention of urinaryphosphate stonedevelopment, bindingof phosphate inchronic renal failure

Symptomatic relief ofgastric irritation,hyperphosphatemia inchronic renal failure

Symptomatic relief ofgastric irritation, cal-cium supplementation

Symptomatic relief ofgastric irritation,hypomagnesemia,constipation

Symptomatic relief ofgastric irritation

GERD, PUD, acid hyper-secretory states




Reflux esophagitis,treatment of gastricand duodenal ulcers,pathological hyper-secretory states(Zollinger-Ellison syndrome)

Fecal impaction,cramps, constipation,hypophosphatemia(when given in exces-sive doses)

Constipation, hypophos-phatemia (when givenin excessive doses)

Headaches

Hypermagnesemia,abdominal crampingand diarrhea (withhigh doses)

Constipation

Confusion, headaches,diarrhea

Headaches, dizziness,constipation

Headaches, dizziness

Dizziness, headaches,diarrhea

Headaches, diarrhea,abdominal pain

Monitor phosphoruslevels.

Less phosphate bindingthan aluminum car-bonate.

Monitor phosphoruslevels.

Usually well tolerated.Monitor calcium and

phosphorus levels.

Monitor magnesium levels.

Use with caution insodium-restrictedpatients.

May cause rare blooddyscrasias.

Monitor CBC.

May cause hepatotoxic-ity and rare blooddyscrasias.

May cause seizures,bronchospasm, con-stipation, or thrombo-cytopenia.

Monitor CBC.

Less common sideeffects include nau-sea, vomiting, anddizziness.

(continued)

4 PART 8 GASTROINTESTINAL SYSTEM

table 40-1 ■ Mechanisms of Action, Indications, Common Adverse Effects, and Comments for Common Gastrointestinal Medications (Continued)


Pancreatic EnzymesPancreatin (Creon,

Donnazyme, Ultrase)

Pancrealipase (Pancrease, Viokase)

AntidiarrhealsAttapulgite (Kaopectate)

Bismuth subsalicylate (Pepto Bismol)

Cholestyramine (Questran)

Loperamide (Imodium)

Tincture of opium (Paragoric, DTO)

LaxativesBowel EvacuantsPolyethylene glycol with

electrolytes (Colyte, NuLytely, GoLYTELY)

Bulk-Forming AgentsCalcium polycarbophil

(Fibercon), methyl-cellulose (Citracel), psyllium (Metamucil)

Nausea, diarrhea,cramping, anorexia,hypersensitivity reactions, perianalirritation

Nausea, diarrhea,cramping, anorexia,hypersensitivity reactions, perianalirritation

Increased potassiumloss, interferencewith absorption ofmedications

Tongue discoloration,dark stools

Constipation

Abdominal distension,constipation, drowsi-ness, dizziness, nau-sea, vomiting

Drowsiness, lighthead-edness, bradycardia

Transient bloating, nau-sea, cramping

Flatulence, impaction (iffeces is obstructed)

Assess electrolytes ifdiarrhea persists.

Use cautiously inpatients using othersalicylates.

Because it may alterabsorption of othermedications, adminis-ter other medicationsat least 1 h beforecholestyramine.

Side effects are relatedto opioid content.

Other possible reac-tions include allergicreactions, vomiting,dizziness, sweating,constipation, andhabituation.

Generally well tolerated.

Replacement in pancre-atic enzyme deficien-cies, cystic fibrosis

Replacement in pancre-atic enzyme deficien-cies, steatorrhea ofmalabsorption, cysticfibrosis, postgastrec-tomy, or postpancrea-tectomy

Diarrhea

Diarrhea, prophylaxis oftraveler’s diarrhea

Diarrhea caused by bilesalts or C. difficile

Acute and chronic diarrhea

Acute diarrhea, relief ofabdominal cramping

Bowel cleansing beforecolonoscopy or bowelsurgery

Diarrhea, constipation

Assistance in the diges-tion of carbohydrates,fats, and proteins

Assistance in the diges-tion of carbohydrates,fats, and proteins

Absorption of toxinsproduced by bacterialand gastrointestinalirritants; decrease ingastric motility andstool water content

Slowing of motility;antimicrobial activityagainst gastrointesti-nal microbes; anti-secretory sensitivity

Absorption of bile salts,which can cause diar-rhea; absorption ofClostridium difficiletoxin

Slowing intestinal motility, includingperistalsis

Decrease in gastro-intestinal motility andperistalsis, decreasein digestive secretions

Nonabsorbable solutionthat acts like anosmotic agent

Nondigestable plant cellwall draws water intothe feces and softensstool; absorption ofexcess water in thestool

(continued)


table 40-1 ■ Mechanisms of Action, Indications, Common Adverse Effects, and Commentsfor Common Gastrointestinal Medications (Continued)


Lactulose (Cephulac, Enulose)

Polyethylene glycol (MiraLax)

Saline LaxativesMagnesium citrate (Citrate

of Magnesium)

Sodium biphosphate (Fleet Phospha-soda, Fleet Enema)

StimulantsBisacodyl (Dulcolax)

Cascara

Senna (Senokot, SenokotXTRA)

Phenolphthalein (Ex-Lax)

Stool SoftenersDocusate sodium

(Surfak, Colace)

Stimulant/Stool SoftenersGlycerin

AntiemeticsTrimethobenzamide

(Tigan)

Hyperosmolality drawswater into the intesti-nal lumen, increasingstool water contentand softening stool;prevention of absorp-tion of ammonia inthe colon

Nonabsorbable solutionthat acts like anosmotic agent

Magnesium and sodiumsalts are poorlyabsorbed, drawingwater into the intesti-nal lumen

Increase in water ab-sorption in the smallintestine throughosmosis

Increase in peristalsis bydirect effect on nerveendings in colonicmucosa

Increase in propulsivemovements throughchemical irritation ofthe colon

Stimulation of propulsion

Stimulation of peristalsis(similar to bisacodyl)

Increase in the penetra-tion of the feces bywater and fat; soften-ing of the stool

Drawing water into thecolon (by highosmotic pressure)

Inhibition of thechemoreceptor triggerzone, which theninhibits the vomitingcenter

Constipation, preven-tion and treatment ofhepatic encephalop-athy

Constipation

Constipation, cleansingof the colon beforeexamination

Constipation, acutebowel evacuationbefore a bowel orcolon examination

Constipation, evacua-tion of bowel beforeexamination

Constipation

Constipation

Constipation

Constipation

Constipation

Symptomatic relief ofnausea and vomiting

Flatulence, cramping,impaction (if feces isobstructed)

Nausea, abdominalbloating, cramping,diarrhea

Cramps, flatulence, nau-sea, vomiting

Nausea, cramps

Discoloration of urine(red or yellow-brown)

Discoloration of urine

Cramping, diarrhea

Headaches, nausea,vomiting

Hypersensitivity, drowsi-ness, hypotension,diarrhea, depression,vertigo

For use in prevention andtreatment of hepatic encephalopathy, titrate dose to two to threeloose stools a day.

Monitor serum ammonialevels.

Do not use in renal disease.

Observe for hypermag-nesemia (watching forthirst, drowsiness,dizziness).

May precipitate or exac-erbate cardiac, renal,or seizure shock dis-order.

Can cause habituationwith gradual lesseningeffect in long-termuse.

PO onset is 6 to 10 h;PR onset is 15 to 60 min.

May cause habituation.Onset is 6 to 10 h.

Natural product fromcassia

May cause an allergicreaction; discontinueuse if rash develops.

Prolonged or excessiveuse may cause habitu-ation or electrolyteabnormalities.

(continued)




Prochlorperazine (Compazine)

Promethazine (Phenergan)

Dolasetron (Anzemet)

Granisetron (Kytril)

Ondansetron (Zofran)

OtherSucralfate (Carafate)

Metoclopramide (Reglan)

Misoprostol (Cytotec)

Other reactions mayinclude thrombocyto-penia, agranulocyto-sis, and hemolyticanemia.

Use with caution inpatients with liver disease.

Because it may alterabsorption of othermedications, patientshould take othermedications at least 2 h before sucralfate.

May occasionally haveextrapyramidal sideeffects.

Use with caution in preg-nant women and inwomen of childbearingage; it increases uterine contractions,which may causeabortion.

Extrapyramidal sideeffects such asdrowsiness, blurredvision, tachycardia,and respiratorydepression

Dizziness, drowsiness,constipation, urinaryretention

ECG changes, hyper-tension, abdominalpain, diarrhea, urinaryretention

Headache, constipation,asthenia

Diarrhea, bronchospasm,fatigue, constipation

Constipation

Diarrhea, constipation,drowsiness, restless-ness

Diarrhea, nausea, vomit-ing, flatulence

Nausea, vomiting

Nausea, vomiting,motion sickness,sedation

Nausea and vomitingassociated withchemotherapy, pre-vention and treatmentof postoperative nau-sea and vomiting

Nausea and vomitingassociated withchemotherapy andradiation

Nausea and vomitingassociated withchemotherapy, pre-vention of post-operative nausea andvomiting

Short-term treatment ofpeptic ulcers

Diabetic gastroparesis,delayed gastric emp-tying, short-termtreatment of GERD,prevention of post-operative nausea andvomiting, facilitationof small bowel feedingtube placement

Prevention of aspirin-and NSAID-inducedulcers

Blocking of dopaminereceptors in thechemoreceptor triggerzone in the brainstem

Competition with hista-mine in blood vesselsand gastrointestinaland respiratory sys-tems to decreaseallergic responses

Blocking serotonin (5-HT3) receptors inthe chemoreceptortrigger zone andgastrointestinal tract



Formation of a protectivecovering at ulcer site

Stimulation of uppergastrointestinal motil-ity; decrease ininhibitory tone

Prostaglandin analogincreases bicarbonateand mucus releaseand decreases acid secretions

(continued)


sources such as proteins), and increases lipolysis (fat break-down and mobilization). Insulin, in contrast, helps trans-port glucose for storage into the cells and tissues, preventsfat breakdown, and increases protein synthesis.

Glycogenolysis is controlled by the hormone glucagonand the catecholamines epinephrine and norepinephrine(which are released from the adrenal medulla in times of stress). Once glucose and glycogen stores have beenexhausted (usually within 8 to 12 hours), hepatic gluconeo-genesis increases dramatically to meet metabolic demands.3Hormones that stimulate gluconeogenesis include glucagonand the glucocorticoid hormone, cortisol. If catabolicprocesses continue without the support of energy, aminoacids, and essential nutrients, depletion of existing bodystores compromises overall bodily health and function, andthe patient progresses toward a malnourished state.

Approximately 15% to 20% of hospitalized patients haveevidence of malnutrition.3 The most important reason to properly nourish patients is to prevent the immuno-suppression and impairment of physiological organ func-tion that result from malnutrition. Malnutrition fromstarvation alone can usually be corrected by replacing bodystores of essential nutrients. However, malnutrition result-ing from critical illness and disease processes that altermetabolism is not as easily rectified.

The degree of starvation and physiological stress deter-mines the extent and type of malnutrition. The threemajor types of protein-energy malnutrition are marasmus,kwashiorkor and protein–calorie malnutrition. Marasmus isa more severe, cachectic process, whereby virtually all of theavailable fat stores have been exhausted from prolongedcalorie deficiency and severe muscle wasting is evident.Despite this, albumin, a visceral protein measurement, maybe within normal limits or only slightly reduced.3 Treatmentrequires slow initiation of nutrition and fluid volume to pre-vent the complications associated with sudden fluid shifts,electrolyte abnormalities, and cardiorespiratory failure.

In contrast to the adaptive response of relative proteinsparing of marasmus, kwashiorkor and protein-calorie mal-nutrition are typically caused by an acute, life-threateningillness, such as surgery, trauma, or sepsis. Kwashiorkortends to be seen in children in developing countries who

have had prolonged periods of protein malnutrition,whereas protein-calorie malnutrition is more commonlyseen in developed countries and is due to depletion of fat,muscle wasting, and micronutrient deficiencies from acuteand chronic illness. Typically, during periods of high acu-ity when the patient is relegated to NPO status (nil per os,nothing by mouth) for surgery, diagnostic testing, or anumber of other medical complications, hypermetabolismincreases protein and energy demands. Although the criti-cally ill patient may appear nourished, this is often due tothe masking effects of generalized edema—the result ofextracellular fluid shifts caused by low-protein oncotic pres-sures in the intravascular space. Other than edema, clinicalsigns of protein malnutrition include skin breakdown, poorwound healing, surgical dehiscence, or a combination of thethree. Additionally, hair can easily be plucked, and hairremnants are often noted on the patient’s pillowcase andsheets. Laboratory data reveal low serum albumin levels,and treatment requires aggressive repletion of proteinstores.3 The fact that protein malnutrition is much easierto prevent than to treat reinforces intense nursing vigi-lance over the patient’s nutrition status.

Both marasmus and kwashiorkor can coexist. Typically,this is seen when a marasmic patient is exposed to an acutestressor such as surgery, trauma, or sepsis. Although eachsituation must be evaluated individually, aggressive pro-tein and calorie replacement is often indicated. Regardlessof the type or types of malnutrition, vigilant monitoring iscrucial to the success of nutrition therapy.

A nutritional assessment should be completed on all crit-ically ill or injured patients early in their hospitalization todetermine the need for nutritional support. Goals of care innutritional support include the following: prevention andtreatment of macronutrient and micronutrient deficiencies,maintenance of fluid and electrolyte balance, prevention ofinfection and other complications associated with nutri-tional support, and improvement of patient morbidity andmortality. Meeting these goals involves a multidisciplinaryapproach that includes the nurse, physician, dietitian, andpharmacist. Sample nursing diagnoses and collaborativeproblems are given in Box 40-1. After a dietitian deter-mines nutritional needs, a method of delivering nutritional



Octreotide (Sandostatin)

CBC, complete blood count; GERD, gastroesophageal reflux disease; NSAIDs, nonsteroidal anti-inflammatory drugs;PUD, peptic ulcer disease.

Monitor blood sugarsand adjust insulinrequirements.

Edema, flushing, dizzi-ness, headache,abdominal pain, con-stipation, diarrhea,hyperglycemia, hypo-glycemia

Secretory diarrhea, acutevariceal hemorrhage

Synthetic analog ofsomostatin, inhibitionof the secretion ofgastrin, vasoactiveintestinal peptide (VIP), insulin, glucagon, motilin, secretin, andpancreatic poly-peptides

supplementation must be selected. In patients unable tomeet their nutritional needs with oral intake, nutritionalsupplementation may be delivered by either enteral or par-enteral routes. Figure 40-1 outlines the decision-makingprocess. Considerations for special populations are givenin Boxes 40-2 and 40-3.

ENTERAL NUTRITION

Enteral nutrition refers to any form of nutrition deliveredto the gastrointestinal tract. For those patients with anintact gastrointestinal tract, the enteral route is the pre-ferred method of nutritional support. A clinical rule ofthumb is, “if the gut works, use it.”

The gastrointestinal mucosa depends on nutrient deliv-ery and adequate blood flow to prevent atrophy, therebymaintaining the absorptive, barrier, and immunologicalfunctions of the intestine.4–6 Enterocytes are tightly packedepithelial cells that line the intestinal lumen and function asa barrier to bacterial invasion. Gut-associated lymphoid tis-sue (GALT) lines the gastrointestinal tract and is associatedwith maintenance of the immunological function of themucosa.4 GALT produces immunoglobulin A (IgA), whichis secreted across the gastrointestinal mucosa, preventingbacterial adherence to the enterocytes.4,7 Without food, thegastrointestinal mucosa atrophies. As a result of atrophy,the tissue available to absorb nutrients decreases, andGALT is impaired. Preservation of the intestinal mucosalintegrity is also essential to preserve its function as a barrier.With atrophy, there is a loss of the tight junctions betweenenterocytes, resulting in increased mucosal permeabilityand decreased barrier function.4,7,8 This decreased bar-rier function can allow resident gastrointestinal bacteriaand endotoxins to enter the systemic circulation. Thisprocess, called bacterial translocation, can trigger immuneand inflammatory responses that can lead to infection,sepsis, and multisystem organ failure.4,9 In addition to itstrophic effects on the gastrointestinal tract, enteral nutri-tion is associated with enhanced utilization of nutrients,decreased infectious complications, ease and safety ofdelivery, and lower cost.

Enteral nutrition is considered when the patient cannotor should not eat, intake is insufficient or unreliable, the

patient has a functional gastrointestinal tract, and accesscan be safely achieved. Mechanical obstruction is the onlyabsolute contraindication to enteral feedings. Relative con-traindications include severe hemorrhagic pancreatitis,necrotizing enterocolitis, prolonged ileus, severe diarrhea,protracted vomiting, enteric fistulas, and intestinal dys-motility.8 Each situation should be evaluated individually.

Enteral nutrition can be delivered through feedingtubes placed into the stomach or the small intestine. Theexpected duration of nutritional support, the patient’soverall condition, risk of aspiration, function of the gastro-intestinal tract, and placement technique should all beconsidered when deciding on which type of feeding tubeto place. Oral enteric tubes are a good choice for neonateswho are obligate nose breathers to avoid airway compro-mise, but for most other patient populations, nasoenterictubes are more widely used.10

Methods of Enteral Nutrition DeliveryNASOENTERAL FEEDING TUBESA nasoenteric tube is indicated for short-term use, usuallyless than 30 days. Nasoenteral tubes are inserted throughthe nose and advanced through the esophagus into thestomach (nasogastric tube), the duodenum (nasoduodenaltube), or jejunum (nasojejunal tube). The tube is identifiedby the distal location of its tip. Most nasoenteric tubes aresoft, flexible, small-bore polyurethane or silicone tubesthat are 8 to 14 French in diameter, 20 to 60 inches inlength, and radiopaque to allow for radiographic confir-mation of placement. The shorter lengths are used fornasogastric feedings, and the longer for nasoduodenal ornasojejunal feedings. As a general rule, the smallest-diameter tube of appropriate length is preferred becausethe smaller diameter has been associated with less compli-cations and increased patient comfort. Small-diametertubes may help to prevent reflux and lessen the risk of aspi-ration because the small diameter lessens compromise of the lower esophageal sphincter (LES). In addition,small-diameter tubes cause less inhibition of swallowing,which is more comfortable for patients. Tubes made ofpolyvinyl chloride are less desirable because, over time,they can stiffen in the presence of acid, which can lead topatient discomfort and increased complications (such astube perforation).10 Any nasally placed tube can causesinusitis, erosion of the nasal septum or esophagus, epi-staxis, or distal esophageal strictures, which may limitlong-term use. Small, soft-bore tubes are less likely tocause these complications.

Most nasoenteric tubes have multiple ports staggeredalong their sides and tip, which minimize clogging andmaximize flow. Many devices also have weighted tips and a stylet, which stiffens the tube to assist in place-ment. Another common feature of many nasoenterictubes is a “Y port” at the proximal tip, which allows forthe administration of medications and irrigation withoutinterrupting tube feeding.

Types of Nasoenteric TubesNasogastric Tubes. Gastric feedings through a naso-

gastric tube are appropriate for patients who have intactgag and cough reflexes and adequate gastric emptying.


box 40-1 Examples of Nursing Diagnosisand Collaborative Problems for the PatientWith Gastrointestinal Problems

■ Imbalanced Nutrition: Less than Body Requirements■ Imbalanced Nutrition: More than Body Requirements■ Risk for Aspiration related to reduced level of con-

sciousness, depressed cough and gag reflexes, incom-petent lower esophageal sphincter, delayed gastricemptying, displaced feeding tube

■ Diarrhea related to altered dietary intake, malabsorption,concomitant drug therapy, type of formula, bacterialcontamination, stress/anxiety

■ Risk for Infection related to invasive procedure anddelivery of high concentrations of glucose parenterally


Nasogastric tubes usually range from 8 to 12 French indiameter and 30 to 36 inches in length. Small-caliber naso-gastric tubes are used solely for feeding, whereas large-caliber tubes can be used to decompress the stomach,monitor gastric pH, and deliver medications and feedings.Large-caliber nasogastric tubes are usually made of stiffer

material and are often less comfortable for patients, possi-bly triggering self-extubation. These tubes are usually usedto decompress and drain the stomach temporarily and aretherefore typically for short-term use.

Advantages to gastric feeding include the ease of place-ment, the ease of checking residuals, and patient tolerability

figure 40-1 Route of administration of specialized nutrition support. Adapted from ASPEN Clinical Pathways andAlgorithms for Delivery of Parenteral and Enteral Nutrition Support in Adults. (Source: Jacobs D (ed): Section II: Nutri-tion Care Process. Journal of Parenteral and Enteral Nutrition 26 (1 Suppl): 85A, 2002.)*Formulation of enteral and parenteral solutions should be made considering organ function (e.g., cardiac, renal,respiratory, hepatic).†Feeding may be more appropriate distal to the pylorus if the patient is at increased aspiration risk.**Elemental low-/high-fat content, lactose-free, fiber-rich, and modular formulas should be provided according tothe patient’s gastrointestinal tolerance.‡Polymeric, complete formulas, or pureed diets are appropriate.

during enteral infusions. However, patients with naso-gastric tubes are at the greatest risk for aspiration, especiallywhen they are unconscious, mechanically ventilated, orotherwise unable to protect their airway. In a consciouspatient, the mere physical appearance of the tube andassociated discomfort may limit the clinical use of naso-gastric tubes.

Nasoduodenal Tubes and Nasojejunal Tubes. Naso-duodenal tubes and nasojejunal tubes are thought to bebetter suited for long-term use than nasogastric tubes.Nasoduodenal tubes and nasojejunal tubes are advancedthrough the stomach, past the pylorus, and into the smallintestine, usually in the third portion of the duodenumbeyond the ligament of Treitz. In theory, the pyloricsphincter provides a barrier that lessens the risk of aspira-tion or regurgitation.

Many critically ill patients and those with medicalissues, such as diabetes, renal dysfunction, or spinal cordinjuries, may have delayed gastric emptying. Transpyloricfeeding can be given without regard to gastric emptying,providing an additional advantage over intragastric feeding.Candidates for transpyloric feedings include critically illpatients with a prior history of gastric aspiration, patients atrisk for aspiration (such as ventilated patients), and patientswith neurological conditions who are unable to protecttheir airway.

A common misconception is that enteral feedings shouldnot be started if bowel sounds are absent. Bowel sounds arean indication of gastrointestinal motility, not of absorption.Postinjury and postoperatively, bowel sounds may not bedetected for 3 to 5 days owing to gastric atony. The smallbowel is less prone to ileus than the stomach or the colonand retains its absorptive and digestive capabilities, mak-ing it possible to accept enteral feedings immediately aftersurgery or trauma.11

Nasoduodenal tubes and nasojejunal tubes range from8 to 14 French in diameter and 46 to 60 inches in length.The length and diameter make it more difficult to checkfeeding residual because the lumen is smaller and tends tocollapse on itself when aspirated. In addition, clogging ofmedications is more common than with nasogastric tubes.The primary disadvantage associated with nasoduodenaland nasojejunal tubes relates to the difficulty in initiallyplacing the tubing tip past the pyloric sphincter.

Placement of Nasoenteric TubesIn most intensive care units (ICUs), trained nurses or

physicians routinely place nasoenteric tubes. Before plac-ing a feeding tube, the nurse refers to institution policyand protocol because nasoenteric tube placement hasmany potential complications. Patients with a decreasedlevel of consciousness, poor cough or gag reflex, or aninability or unwillingness to cooperate are at increased riskfor pulmonary intubation. When a patient cannot coop-erate or cough when the tube enters the bronchial tree,the nurse must take extra precautions to ensure properplacement. Feeding tubes placed in the bronchial tree cancause pulmonary hemorrhage or pneumothorax. Neverassume a cuffed endotracheal tube precludes accidentalpulmonary intubation. Nasoenteric tubes can also be acci-dentally placed in the esophagus or, in patients with basi-lar skull fractures, in the intracranial space.


box 40-2

Nutritional Care of the Pediatric Patient

■ Address all the child’s questions and explain all theprocedures according to the child’s developmentallevel.

■ Involve the child (if old enough) in his or her nutritionalcare.

■ Allow the parents to assist as much as possible.■ Pediatric patients have a greater need for many nutri-

ents, so consider age, weight, size, activity level, anddevelopment when administering solution components.

■ Pediatric patients are particularly susceptible to fluidoverload; therefore, be careful to administer the cor-rect volume and infusion rate.

■ Monitor intake and output and weight daily.■ Provide written educational material for the parents for

review and reinforcement.

box 40-3

Nutritional Requirementsin the Older Patient

■ The risk for malnutrition increases as functional abilitiesdecrease.

■ The caloric needs of the elderly are generally less, secondary to decreased metabolism.

■ Although protein requirements remain the same, it isimportant to monitor renal function.

■ There is decreased ability to tolerate glucose loads.■ Atrophic gastritis occurs frequently in the elderly,

which can result in decreased gastric acid secretion.The resultant achlorhydria or hypochlorhydria canlead to bacterial overgrowth and altered absorptionof iron, vitamin B12, folate, calcium, vitamin K, andzinc.

■ Lactose intolerance increases with age; this intoleranceto dairy products can contribute to osteopenia.

■ Vitamin D deficiency in the elderly can be due todecreased dietary intake, decreased synthesis, ordecreased exposure to sunlight.

■ The elderly have less ability to regulate fluid balance,which places them at an increased risk for dehydrationor overhydration.

■ Encourage increased dietary fiber, fluids, and exerciseto reduce the incidence of constipation.

■ Decreased gastrointestinal motility, exocrine function,and digestion or absorption may occur in the elderly.

■ Physical changes in the jaw, including poor dentition orpoorly fitting dentures, may interfere with masticationand adequate food intake.

■ Swallowing may be more difficult because of de-creased esophageal motility and decreased saliva production.

■ Multiple medications or concomitant disease may con-tribute to anorexia or diminished sense of taste.


Nasogastric tube placement is usually easier than naso-duodenal or nasojejunal tube placement. When placing anasoenteric feeding tube in the stomach, determine thelength of tube insertion by measuring the distance fromthe tip of the nose, to the earlobe, to the tip of the xiphoidprocess. Before insertion, consider using a topical anes-thetic or water-soluble lubricant to assist in placement.After placing the patient’s bed in a high Fowler’s position,slightly flex the patient’s head (if not clinically contraindi-cated), and pass the lubricated tip through the nares intothe nasopharynx. Ask the patient to swallow repeatedlywhile advancing the tube. Having the patient sip waterthrough a straw may also assist in tube placement (if not clinically contraindicated). Rotating the tube as it isadvanced may also ease advancement.

When attempting to pass the nasoenteric tube tip pastthe pylorus, follow the same procedure described previously,then turn the patient to the right lateral decubitus positionto take advantage of gravity and peristalsis. To get the tipof the feeding tube past the pylorus into the small bowel, thelength of the tube should be at least 40 inches.12 Nasoduo-denal and nasojejunal tubes depend on gastric motility tocarry the tip through the pylorus, but have a tendency to coilin the stomach. Some nasoduodenal tubes and nasojejunaltubes have weights to aid in passage through the pylorus;however, the utility of the weighted tip is dubious. A pro-motility agent such as metoclopramide or erythromycin maybe ordered before insertion. These medications increaseupper gastrointestinal motility while relaxing the pylorus.Air insufflation, the process of inserting large amounts of airinto the stomach, may also be helpful by distending thestomach and facilitating tube passage though the pylorus.9 Ifpassage of a nasoduodenal or nasojejunal tube does notoccur within 24 hours, endoscopic or radiological assistanceshould be sought to advance the tip of the tube.

Before initiating tube feeding, proper tube placementmust be confirmed by an abdominal radiograph. Feedingtubes placed surgically, by endoscopy, or under fluoroscopydo not require radiographic confirmation of placement.The external length of the tube is documented after place-ment is confirmed. Mark the tube with tape or indelibleink at the point it enters the nares. Recheck tube place-ment before initiating intermittent feedings or medicationadministration, and at least once each shift. Monitor tubeplacement during continuous tube feeding according to theinstitution’s policy.

Auscultation, aspiration and inspection of aspirate, andpH testing may all be used to monitor tube placement afterinitial placement is confirmed by an abdominal radiograph.No one method is infallible, so using a combination of thesemethods is advised.4 Injecting air into the tube and auscul-tating the gastric bubble, although commonly used, is notan accurate method to verify initial tube placement. An airbubble sound can be transmitted to the epigastrium whenthe tube is in the esophagus. Although auscultation of insuf-flated air is not a reliable method to confirm initial feedingtube placement, it may still provide useful information. Ifno resistance is met, the tube is unlikely to be kinked, and,if the patient immediately burps back air, the tip of the tubeis probably in the esophagus.12

Aspiration and inspection of the aspirate may help todifferentiate between gastric and intestinal placement,

but not between intestinal and pulmonary placement.Fluid aspirated from the stomach is usually cloudy green,tan, brown, or bloody.4,10,11 Small intestinal aspirate isusually yellow, clear, or bile colored. Pulmonary fluid isusually tan, white, clear, or pale yellow and can closelymimic gastric or intestinal aspirates.4,10,11

Measuring the pH of fluid aspirated from the feedingtube is another method of monitoring tube placement.Keep in mind that the diameter of small intestinal tubesmay not allow withdrawal to check aspirate. Aspirate witha pH of less than 4.0 is highly predictive of gastric place-ment.12,13 However, the pH of gastric aspirate can be ele-vated with the infusion of enteral formulas, the use ofacid-modifying medications, and the presence of bile reflux.The pH of both small intestinal aspirate and pulmonaryfluid is usually greater than 6.0; therefore, if the pH of theaspirate is greater than 4.0, tube position cannot be deter-mined based on pH alone.12,13

Suctioning and patient movement or coughing maypotentially dislodge a feeding tube. If at any time tubelocation is in question, hold the tube feeding and obtainan abdominal radiograph to confirm placement.

Securing Nasoenteric TubesBefore securing any feeding tube, clean the skin with

alcohol to remove oils and dirt and consider applying a skinprotectant to maintain skin integrity. Nasoenteric tubesshould be secured in a way that avoids irritation or pressureof the nares, thus preventing necrosis. Allow the tube tohang straight from the nares and secure it to the bridge ofthe nose or the cheek with tape (or one of the many com-mercially available devices). For agitated or uncooperativepatients, consider soft wrist restraints or mitts to avoid acci-dental self-extubation. The institution’s policy and proce-dure should be referred to regarding the use of restraints.The skin and nostrils should be inspected every 4 to 8 hoursfor signs and symptoms of irritation, erythema, or skinbreakdown. Patient comfort can be maximized by provid-ing frequent mouth care and moistening of the nares.

ENTEROSTOMAL FEEDING TUBESIf therapy is expected to last a month or more, a morepermanent enterostomal device can be inserted throughthe abdomen into the stomach (gastrostomy) or jejunum(jejunostomy; Fig. 40-2). Enterostomal feeding tubes arealso indicated when the nasal route is contraindicated andin patients with impaired swallowing or obstruction ofthe oropharynx, the larynx, or esophagus. Enterostomaltubes are made of silicone and polyurethane and are verydurable.

Types of Enterostomal Feeding TubesGastrostomy Tubes. Gastrostomy tubes may be used

temporarily or for permanent feeding. If a gastrostomy tubeis intended for permanent feedings, it may need to bereplaced as the tube material deteriorates over time. Gas-trostomy tubes may also be used for chronic gastric decom-pression. A low-profile gastrostomy device (LPGD), oftenreferred to as a button, may be used to replace gastrostomytubes in a mature gastrostomy tract, usually 3 to 6 monthsafter initial placement or as an initial placement.10 LPGDsare anchored in the stomach and protrude through the

abdomen, flush with the skin. These devices require a spe-cial extension adapter to connect with the tube-feeding bag,to check for residuals, and to use for decompression. Thisadapter may then be removed after use. Some LPGDs areequipped with a one-way antireflux valve to prevent leakageof gastric contents onto the skin. These devices are usuallywell accepted because they are durable, unlikely to irritatethe skin, and difficult to dislodge. With agitated or confusedadults who have a tendency to pull on their tubes, theseadvantages may be of benefit.

Jejunostomy Tubes. When gastric feedings are notpossible or desired, jejunostomy tubes (J-tubes) are pre-ferred for long-term feeding. J-tubes deliver enteral for-mula past the duodenum into the jejunum, decreasingpancreatic stimulation. J-tubes are indicated in patients whowill benefit from jejunal feeding, such as those with gastricdisease, abnormal gastric emptying, upper gastrointestinalobstruction or fistula, pancreatitis, or decreased gag reflexwith significant risk of aspiration. J-tubes are contraindi-cated in patients with primary diseases of the small bowel(such as Crohn’s disease) or radiation enteritis because theymay increase the risk of enterocutaneous fistula forma-tion.11 A limitation of J-tubes is the potential for obstruc-tion due to the small diameter of the lumen.

Placement of Enterostomal TubesPercutaneous endoscopic, open surgical, laparoscopic,

and fluoroscopic techniques may be used to place a gas-

trostomy tube. J-tubes may be placed by percutaneousendoscopy or surgical methods. The patient’s underlyingdisease and physician expertise need to be consideredwhen selecting the appropriate placement technique.

Percutaneous Endoscopic Gastrostomy. Percutaneousendoscopic gastrostomy (PEG) has rapidly become thepreferred method for placement of gastrostomy devices.A PEG may be done at the bedside or in the endoscopysuite, using minimal sedation. Other advantages of PEGplacement include increased comfort, decreased cost, anddecreased recovery time. A candidate for a PEG musthave an intact oropharynx and an esophagus free fromobstruction. The only absolute contraindication to PEGplacement is the inability to bring the gastric wall intoapposition with the abdomen. Prior abdominal surgeries,ascites, hepatomegaly, and obesity may impede gastric trans-illumination and preclude the placement of a PEG.

Complications of PEG are infrequent but include woundinfection, necrotizing fasciitis, peritonitis, and aspiration.Pneumoperitoneum, a common finding after PEG place-ment, is not clinically significant unless accompanied bysigns and symptoms of peritonitis.6 Prophylactic antibioticsare usually given 30 to 60 minutes before procedure. Cor-rect placement is then verified by endoscopy.

In patients with severe gastroesophageal reflux disease,gastroparesis, or aspiration related to tube feeding, a PEGcan be modified with a jejunal extension tube known as aPEG/J tube. The gastric lumen of a PEG/J tube is usuallyused for gastric decompression, and the jejunal lumen isused for the simultaneous delivery of enteral feeding.PEG/J tubes may decrease the risk of gastric aspiration;however, they do not necessarily provide the same pro-tection against aspiration as jejunal tubes because thepylorus is compromised by the large catheter.11 The jeju-nal portion of a PEG/J tube may migrate back into thestomach and increase the risk of occlusion, gastric reflux,or aspiration. Both PEG and PEG/J tubes are held inplace by internal and external retention devices. Theinternal device rests in the stomach, which preventsmigration and leakage of gastric contents. The externalretention device anchors the tube to the abdomen.

Surgical Gastrostomy. Surgical gastrostomy tubes areinserted through an incision in the abdominal wall undergeneral anesthesia. The stomach is usually sutured to theabdominal wall to create a permanent connection betweenthe gastric and abdominal wall. Surgical placement of a gas-trostomy is usually chosen if the surgeon wants to view thegastric anatomy clearly or as a secondary procedure duringabdominal surgery. Disadvantages of surgical placementinclude increased recovery time, decreased comfort, andincreased cost.

Laparoscopic Gastrostomy. A laparoscopically placedgastrostomy tube also requires general anesthesia or intra-venous (IV) conscious sedation. Laparoscopic placement isusually reserved for patients with head, neck, or esophagealcancer. It is less invasive, less painful, and usually involvesless complications than a surgical gastrostomy.

Fluoroscopic Gastrostomy. Direct percutaneous cathe-ter insertion of a gastrostomy tube under fluoroscopy is indicated with high-grade pharyngeal or esophageal


figure 40-2 Possible routes for feeding. PEG, percutaneousendoscopic gastronomy; PEG/J, PEG modified with a jejunal exten-sion tube; PEJ, percutaneous endoscopic jejunostomy; LPGD, low-profile gastrostomy device.


obstruction. Disadvantages to the use of fluoroscopy toplace enterostomal devices include the inability to detectmucosal disease, the potential for prolonged exposure toradiation, the necessity of transport to the fluoroscopy suite,and increased cost.

Securing Enterostomal Tubesand Caring for the Enterostomy SiteEnterostomal tubes are secured to the abdominal wall

to prevent dislodgment or migration of the tube, to avoidtension on the tubing, and to prevent the external reten-tion device from digging into the skin. The length of theexternal tubing is documented to monitor for migration ofthe tubing.

To avoid maceration, the insertion site is kept cleanand dry by leaving it open to air (unless draining), and lift-ing or adjusting the tube is avoided for several days afterthe initial insertion. To avoid pulling the internal reten-tion device taut against the gastric or intestinal mucosa,the amount of dressing between the device and the skin islimited. A cotton-tipped applicator is used to clean anyaccumulated drainage with half-strength peroxide.11,12

If no drainage is present, cleansing with soap and wateris adequate. The skin around the insertion site and theretention device is assessed at least daily for skin break-down, erythema, or drainage. The tissue usually healswithin a month.11

In-and-out play on the tubing is checked; it should beable to move one quarter of an inch to prevent erosion ofgastric or abdominal tissue.11,12 If the anchor is too tight,the nurse should notify the physician immediately becausethis may indicate “buried bumper syndrome,” a situationwhere the retention device is imbedded in the tissue,thereby leading to mucosal or skin erosion. If a gastros-tomy tube becomes accidentally dislodged, the nurseshould notify the physician immediately so the tube can bereinserted quickly before the tract closes.

Types and Delivery of Enteral FormulasWhen selecting a tube feeding formula, nutrient require-ments, the patient’s clinical status, location of enteralaccess, gastrointestinal function, cost, and duration mustall be considered. There are numerous tube feeding solu-tions available for enteral nutrition, with many designedto assist in the management of specific disease processes;however, no single formula is ideal for all patients. Allcontain proteins, carbohydrates, fats, vitamins, and traceminerals. The difference lies in how these nutrients arestructured and delivered. The dietary formula selected isbased on the patient’s ability to digest and absorb majornutrients, the total nutrient requirements, and fluid andelectrolyte restrictions. Classifications of enteral formulasinclude polymeric, peptide (elemental), and modular:

■ Polymeric solutions are isotonic, and can provideenough protein, carbohydrate, fat, vitamins, traceelements, and minerals to prevent nutritional defi-ciencies. They are considered nutritionally completeif given in enough volume to meet caloric needs.14

Standard formulas deliver 1 kcal/mL, but some con-centrated formulas may provide 2 kcal/mL.8,14,15 The

carbohydrates in polymeric solutions are oligosac-charides and polysaccharides that require pancreaticenzymes for digestion.15 All polymeric solutions con-tain intact proteins (most often meat, whey, milk, orsoy proteins) that require normal pancreatic enzymesfor digestion.8,14,15

■ Peptide (elemental) formulas provide proteins asdipeptides, tripeptides, or oligopeptides and freeamino acids from hydrolysis of whey, milk, or soyproteins.14 These proteins do not require pancreaticenzymes for digestion.14 Elemental solutions are usedwhen digestion is impaired, as in pancreatic insuffi-ciency, radiation enteritis, Crohn’s disease, or shortbowel syndrome secondary to surgical resection.8,14

Elemental solutions have no proven advantage inpatients with normal gut function, are usually moreexpensive than polymeric formulas, and have an un-pleasant taste.14,15

■ Modular formulas contain individual nutrient compo-nents that can be mixed or added to other formulas toindividualize feedings to a patient’s specific nutritionalneeds. The involvement of a dietitian is essential in thepreparation of these formulas because improper mix-ing can result in metabolic abnormalities.

When initiating enteral tube feedings, most cliniciansrecommend beginning with an isotonic formula at a slowrate and increasing the rate incrementally every 8 to 12 hours until the goal rate is achieved. Dilution of formulamay help assist in tolerance but is not recommendedbecause this may increase the time needed to meet thenutritional requirements.

Enteral feedings can be administered by bolus, gravityinfusion, intermittent infusion, continuous infusion, orcyclic infusion. The tube tip location and tolerance gen-erally dictate formula delivery. Gastric feedings are appro-priate for patients who have intact gag and cough reflexesand adequate gastric emptying.

BOLUS FEEDINGSBolus feedings, considered the most natural method phys-iologically, are given by a large syringe in volumes as highas 400 mL over 5 to 10 minutes, five to six times a day.4,8

The stomach is the preferred site for bolus feedings. Thestomach and pyloric sphincter regulate the outflow of feed-ing from the stomach. Bolus feedings allow for increasedpatient mobility because the patient is free from a mechan-ical device between feedings. Unfortunately, as a result ofhigh residuals, bolus feedings are usually not well toleratedand are often accompanied by nausea, bloating, cramping,diarrhea, or aspiration.

INTERMITTENT FEEDINGSIntermittent feedings of 300 to 400 mL are administeredby slow gravity drip or infusion four to six times a day overa period of 30 to 60 minutes. The stomach is the preferredsite for intermittent infusion because of its capacity. Inter-mittent feedings are associated with a decreased risk ofosmotic diarrhea. Disadvantages of intermittent feedingsinclude the dependence on a mechanical device and apower source, which can increase cost and decrease patientmobility.

CONTINUOUS FEEDINGSIf the tip of the nasoenteric tube is in the duodenum orjejunum, tube feedings must be delivered by infusion. Con-tinuous infusions are administered over 24 hours with theaid of a feeding pump to ensure a constant flow rate. Con-tinuous pump feedings are the preferred method for intesti-nal feeding because delivery that is too rapid may lead to“dumping syndrome,” characterized by osmotic diarrhea,abdominal distension, cramps, hyperperistalsis, lighthead-edness, diaphoresis, and palpitations.11,12 When the tube isplaced in the third portion of the duodenum, past the lig-ament of Treitz, continuous pump feedings are associatedwith decreased risk of aspiration. If the feeding is advancedslowly, the small bowel can usually tolerate feedings at arate of 150 mL/hour.10 The continuous method is bestsuited to the critically ill patient because it allows moretime for nutrients to be absorbed in the intestine. Contin-uous infusion is also often used in the ICU because there isdecreased incidence of gastric distension and potential foraspiration.6 Continuous-infusion tube feeding may also actprophylactically to prevent stress ulcers and metabolic com-plications. As with intermittent feedings, disadvantagesinclude the dependence on a mechanical device and a powersource.

CYCLIC FEEDINGSCyclic feedings are continuous feedings that deliver thetotal daily nutritional requirements in a shorter time frame,typically over 8 to 12 hours, to allow the patient freedomfrom 24-hour continuous feedings.4 Cyclic feedings ofhigh density and high volume are typically given at night.This schedule may assist the patient in progressing fromenteral to oral consumption.

The ultimate goal is for patients to resume adequateoral intake. Enteral feeding may be discontinued whenpatients can drink enough liquid to maintain hydrationand can eat two thirds of their nutritional requirements.

Complications of Enteral NutritionAlthough enteral nutrition is in general associated withfewer complications than parenteral nutrition, complica-tions still may occur. These complications generally fallinto gastrointestinal, mechanical, metabolic, and infectiouscategories. Many of these complications can be preventedor treated by closely observing residuals and watching forsigns and symptoms of gastric intolerance.

GASTROINTESTINAL COMPLICATIONSThe patient’s tolerance to enteral feeding depends on therate of flow and the osmolality of the formula. Signs andsymptoms of gastrointestinal intolerance to enteral feedinginclude diarrhea, nausea, vomiting, abdominal discom-fort, distension, and high residual returns. Food nor-mally passes through the stomach at a rate of 2 to 10 mL/minute; however, gastric emptying is delayed or absentin many critically ill patients.13 Unlike the stomach, thesmall intestine cannot act as a reservoir. If large residu-als are withdrawn through a nasoduodenal tube or naso-jejunal tube, the tube may have moved back into thestomach, and placement should be confirmed with anabdominal radiograph.

High ResidualsHigh gastric residuals can also be problematic; however,

consensus about what constitutes a high gastric residualvaries. Recommendations for the cessation of tube feedingfor high gastric residuals also vary widely. Many cliniciansstop tube feeding inappropriately, based on a single highresidual of greater than 200 mL from a nasogastric tubeor greater than 100 mL from a gastrostomy tube.4,8,13

Although this should raise suspicion of intolerance, onehigh residual does not mean feeding failure, and automaticcessation of feeding can delay the patient’s ability to meethis or her nutritional goals. Be sure to evaluate the clinicalstatus of your patient before stopping tube feeding solelyon the basis of one high residual; the key is to monitor sub-sequent volume residuals.

If cessation of tube feedings for high residuals is nec-essary, a common intervention involves holding thefeeding for 1 to 2 hours and rechecking the residualevery 1 to 2 hours until the residual is less than 200 mLfrom a nasogastric tube or less than 100 mL from a gas-trostomy tube, at which point feedings can be resumed.This allows time for normal gastric emptying and reducesthe risk for aspiration. Remember that high infusionrates result in higher residual volumes. The institution’spolicy and protocol regarding high gastric residuals shouldbe checked.

Nausea, Vomiting, and BloatingNausea, vomiting, and bloating are commonly associ-

ated with enteral feedings. Medications, rapid infusion rate,or improper tube placement may cause both nausea andvomiting. Nausea, vomiting, and bloating are most likely tooccur when gastric emptying is delayed. A careful assess-ment of medications that may contribute to these symp-toms should be undertaken, and the medication should beeliminated, if possible. A change of formula, reduction inrate, or addition of a prokinetic agent may also help in themanagement.

DiarrheaDiarrhea is the most common complication of enteral

feedings; however, it is important to consider other etiolo-gies before assuming that enteral feedings are the cause ofdiarrhea. Diarrhea in a patient receiving enteral feedingmay result from the use of antibiotics or other diarrhea-inducing medications; altered bacterial flora; formula com-position; intolerance to lactose, fat, or osmolality; a rate ofinfusion that is too high; hypoalbuminemia; or enteral for-mula contamination.

The liquid form of many medications may containhypertonic sorbitol, which can have laxative effects. Anti-biotics, antacids, magnesium, and prokinetic medicationscan also contribute to diarrhea.7 Antibiotics can contributeto diarrhea by causing bacterial overgrowth of Clostridiumdifficile. To assess for C. difficile infection, a stool sampleshould be assessed for C. difficile toxin. Treatment optionsinclude antibiotic therapy with oral metronidazole, van-comycin, or cholestyramine (a bile acid sequestrant thatbinds the toxin). A patient who has received antibioticsshould not receive antidiarrheals until C. difficile infectionhas been ruled out because diarrhea helps eliminate thetoxin from the intestinal mucosa.



Bacterial overgrowth may cause diarrhea. Reduced gas-tric and small bowel motility may lead to small intestinalovergrowth, which can alter intestinal microflora. Acidsuppression may also permit bacterial overgrowth becausebacteria can colonize the gastrointestinal tract when thegastric pH is greater than 4.0.8

Infusing of enteral feedings too rapidly may cause diar-rhea. Intolerance of lactose, fat, or osmolality may alsolead to diarrhea. Reducing the infusion rate, changing toa peptide-based formula that is easier to digest, and givingan absorbing product, such as Metamucil, may help. Theuse of a fiber-containing formula may be useful in bulkingstools and correction of the diarrhea. Diarrhea can also becaused by bacterial contamination of the solution oradministration set. The nurse checks the expiration dateof the formula and discards the formula if it is expired.Breaks in the system are minimized, and the use of aclosed, prefilled, ready-to-hang solution should be con-sidered. To prevent bacterial contamination, no morethan 4 hours of feeding solution should be hung in thecontainer at one time; any open solution should be usedwithin 24 hours; administration sets should be changeddaily; rinsing should occur between bolus feedings; andgood handwashing technique should be used when han-dling equipment.

In patients receiving enteral feedings, a hyperosmoticformula may also contribute to diarrhea. If diarrheadecreases when the feedings are held, the formula may bethe cause. After consultation with the dietitian, the nurseshould consider changing the formula. Also, a stool sam-ple should be collected to evaluate for an osmotic gap;this may help identify osmotic diarrhea.

Hypoalbuminemia may predispose patients to diarrheaby decreasing the osmotic pressure gradient.13 This de-crease may lead to bowel edema and malabsorption. Anyformula that is not absorbed may contribute to the diar-rhea.13 The prealbumin should be monitored because it isa more reliable indicator of current nutritional status thanserum albumin.

ConstipationConstipation associated with enteral feedings may be

related to poor hydration, lack of fiber, bed rest, impaction,obstruction, and narcotics. Adequate hydration should beensured, and adding a stool softener should be considered,along with minimizing narcotics, encouraging ambulation,and considering the addition of fiber to relieve constipation.

MECHANICAL COMPLICATIONSMechanical complications occur when the tube becomesdislodged, occluded, or malpositioned.

Tube DislodgementTube dislodgment by either patients or staff accounts for

most tube removals. Soft restraints or hand mitts should beconsidered for agitated patients to prevent accidental self-extubation.

Tube CloggingPrecipitation of medications, clogging of pill fragments,

or coagulation of formula may cause obstruction of anyfeeding tube, delaying the administration of nutrients and

medications. To avoid clogging, enteral feeding tubes areflushed every 4 to 6 hours during continuous feeds, beforeand after medication administration, after checking resid-uals, and when turning off feedings. Nasoenteric tubesshould always be flushed with a large, 30- to 60-mL syringeto avoid rupturing the tube with excessive pressure. Theyshould be irrigated with 20 to 30 mL of tepid water.

The enteral solution container should be checkedfrequently for precipitation. Crushed tablets may leavea residual that blocks the tube. To prevent clogging, liq-uid medications should be administered when available.Flushing the tube before and after each medication admin-istration also helps to avoid incompatibilities betweenmedications and feedings and reduces the incidence ofclogging.

An obstruction is suspected if the formula does not flowby gravity, flushing an aspirate from the tube is not possi-ble, or the occlusion alarm of the feeding pump soundsrepeatedly. If an occlusion is suspected, the nurse uses alarge piston syringe to flush the tube with warm water,using a gentle push–pull motion. Although many solutionshave been proposed to assist in clearing an obstructedfeeding tube, they offer no demonstrable benefit over tapwater.4,10,12 A stylet should never be used to unclog a tubebecause of the risk of rupturing the feeding tube andperforating the esophagus, stomach, or small intestine.Recent studies have shown that the pancreatic enzyme,pancrelipase, has been effective in unclogging a tube whenwater is unsuccessful.4,10

METABOLIC COMPLICATIONSMultiple metabolic complications can accompany enteralnutrition. Fluid and electrolyte imbalance may occurbecause of fluid excess, fluid depletion by gastrointestinal orrenal losses, wound drainage, diuresis, fever, or inadequatefree water intake. If dehydration is due to inadequate fluidintake, extra fluid may need to be given by bolus or by auto-matic flush using specialized feeding pumps. The averagepatient with good renal function needs 30 to 35 mL/kgof free water per day, if not otherwise medically contra-indicated.4,8,16 Conversely, if cardiac or hepatic function isimpaired, overhydration from enteral feedings may occur.The determination of the patient’s baseline fluid require-ments and accurate measurement of intake and output canhelp to maintain fluid balance. Keep in mind that many ofthe patients seen in the ICU are often unable to convey feel-ings of thirst, secondary to diminished levels of conscious-ness or intubation.

Hyperglycemia may occur if patients are being overfed,during hypermetabolic states, and as a result of steroidmedications. Blood glucose should be monitored duringenteral therapy; a decrease in formula rate or concentra-tion may help if hyperglycemia occurs. Bolus feeding mayexacerbate hyperglycemia in patients with diabetes. Iffeedings are abruptly stopped, hypoglycemia should beassessed, especially in patients receiving insulin.

INFECTIOUS COMPLICATIONSAspiration of enteral formulas into the lung is a potentiallyfatal complication. Loss of consciousness, mechanical ven-tilation, and many medications used in critically ill patientsincrease the risk of aspiration. To limit this risk, the head of

the bed should be maintained at a 30- to 45-degree angleduring feeding and 1 hour after use; intermittent or contin-uous feedings should be used rather than rapid boluses; gas-tric residuals should be checked frequently; and signs offeeding intolerance should be assessed. Feedings should bediscontinued at least 30 minutes before any procedure forwhich the patient must lay flat.

Pulmonary aspiration, although often subclinical, maybe indicated by a low-grade fever, coughing, shortness ofbreath, rhonchi during or after enteral feeding infusions,and presence of a “sweet” formula odor emanating from thetracheal or oral secretions during suctioning. If the patientis at high risk for aspiration or if there is a clinical suspicionof aspiration, addition of blue dye to the enteral feedingformula is suggested to help visually identify aspirated feed-ing formula. The institution’s policy and protocol should bechecked regarding blue dye administration. Checking tra-cheal suction fluid with a glucose strip and glucometer testsformula aspiration. If the reading is greater than 20 mg/dLor is blue-tinged, aspiration is suggested.13

PARENTERAL (INTRAVENOUS)NUTRITION

There are two types of parenteral (IV) nutrition: central andperipheral. Central parenteral nutrition, also known as totalparenteral nutrition (TPN), is infused through a large cen-tral vein (Fig. 40-3). Peripheral parenteral nutrition (PPN)can be infused into a smaller, peripheral vein owing to thelower osmolarity concentrations. TPN has sometimes beenreferred to as hyperalimentation or “hyperal.” This is not apreferred term because it implies that parenteral nutritiongives more nutrients than the patient may actually require.

Parenteral nutrition is indicated when oral or enteralnutrition is not possible or when absorption or function ofthe gastrointestinal tract is not sufficient (or is unreliable) tomeet the nutritional needs of the patient. Since the incep-

tion of parenteral nutrition in the early 1960s, bowel rest wasthought to be the cornerstone of treatment for many gastro-intestinal disorders. Today, except in cases of severe hemor-rhagic pancreatitis, necrotizing enterocolitis, prolongedileus, and distal bowel obstruction, some enteral nutrition isrecommended to maintain gut integrity and function.3 Ifthe patient has a functioning gastrointestinal tract, if thetreatment is anticipated to last for less than 5 days, or ifprognosis does not warrant aggressive nutrition support,an alternative form of nutritional therapy is suggested.

Methods of Parenteral Nutrition DeliveryTOTAL PARENTERAL NUTRITIONTPN differs from standard IV fluids in that all of the dailyrequired nutrients (carbohydrates, proteins, fats, vitamins,minerals, and trace elements) are delivered to the patient.The solution is infused at a constant rate over a 24-hourperiod to achieve maximum assimilation of the nutrientsand to prevent hyperglycemia (or hypoglycemia). The aimof treatment is a continuous infusion that meets the caloricand nutritional requirements of the patient.

The high osmolarity of TPN formulas requires deliv-ery through a central venous catheter so that the higherblood volumes in larger central veins are able to dilute anddisperse the solution. The superior vena cava is an excel-lent site for such delivery. Passage of the catheter, by wayof the subclavian vein into the superior vena cava, is theroute of choice because it allows the patient the greatestfreedom of movement without disturbing the insertionsite. Jugular veins can also be used, but they are not ascomfortable because of the limitations in neck movement.

Critically ill patients often have issues with reliable IVaccess. Because the TPN formula must be infused sepa-rately owing to the high risk of precipitation and the risk ofcontamination from increased handling, the introduction ofmultiple-lumen catheters has greatly facilitated the care


figure 40-3 Venous anatomy forhyperalimentation routes.


of patients who require multiple IV therapies. Thesecatheters provide separate infusion ports and correspond-ing distal exit sites along the catheter tubing. This preventsdirect mixing of solutions before they are diluted by thehigh blood volumes of the central veins. Therefore, oneport can be dedicated to exclusive use of TPN, while theremaining ports can be used for the administration of IVantibiotics, medications, and blood products, and for bloodsampling. When the central line is a single lumen, thislumen should be used exclusively for the infusion of TPN.

TPN formulas typically contain three primary macronu-trients: carbohydrates, lipids (fats), and amino acids (pro-tein). This combination is called a mixed fuel source. Whenall three fuel sources are combined together in one TPNbag, this is often referred to as a “3 in 1” admixture. Thedesired proportions of these nutrients are prepared by apharmacist under a laminar flow hood to maintain strictsterility. Because of differences in pharmacy equipment tocompound TPN, some agencies infuse lipids separately,usually in a glass bottle. Medications are not to be added toa TPN bag after it has been prepared by the pharmacistbecause of the risk of contamination or precipitation of itscontents. The current trend for TPN formulation is basedon the specific needs of each patient; standard formulas areno longer widely prescribed.

MacronutrientsCarbohydrates. The primary source of energy in the

body is carbohydrates. This macronutrient usually provides40% to 60% of daily caloric requirements and is essentialto central nervous system function. The most common andpreferred source of carbohydrates is dextrose (D-glucose)because it is readily metabolized, stimulates the secretion ofinsulin, and is usually well tolerated in large quantities.Dextrose provides 3.4 kcal/g in IV form and contributes tomost of the osmolality (or concentration) of the TPN solu-tion. Initial concentrations of dextrose may range from50% to 70%, but final concentration is diluted to approxi-mately 25% after the addition of amino acids, lipid emul-sions, and water.3 This final dilution, however, remains veryhypertonic, which can be caustic to smaller blood vessels.To reduce the risk of phlebitis, TPN needs to be infusedthrough a large central vein in which the TPN solution canbe diluted by higher blood volumes.

The amount of dextrose prescribed in TPN is basedon metabolic needs, which, once met, allow utilization ofamino acids for protein synthesis rather than solely as anenergy source. One of the most common metabolic sideeffects of high dextrose concentrations is hyperglycemia,which often requires the use of insulin. In addition, highdextrose concentrations may put certain patients, such asthose with pulmonary compromise, at risk for carbon diox-ide retention and subsequent respiratory acidosis. Becauseone of the end products of dextrose metabolism is carbondioxide, elevated levels may increase minute ventilation andhence the work of breathing. Overfeeding carbohydratesmay make ventilator weaning difficult, if not impossible.

Lipids. Intravenous lipids, or fat emulsions, are long-chain triglycerides from vegetable oils (safflower or soy-bean oils) that are rich in essential and nonessential aminoacids. Lipids provide a concentrated source of calories and

are important in the maintenance of connective tissueintegrity and prevention of fatty acid deficiency. Symp-toms of fatty acid deficiency include dry skin, hair loss,poor wound healing, and diarrhea.17 Lipid concentrationsare available in 10%, 20%, and 30% solutions, providing1.0, 2.0, and 3.0 kcal/mL, respectively. The benefit ofhigher concentrations is that they provide a greater con-centration of calories in less total volume, an importantconsideration in many patients. The usual dose is 0.5 to 1 g/kg/day to supply up to 30% of the patient’s calorieintake; fats are a concentrated energy source providing9 kcal/g. When additional lipid sources such as propofol(Diprivan), a sedative that is delivered as a lipid emulsion,are added, TPN lipid concentrations or quantities mayneed to be adjusted. Because lipid emulsions contain eggphospholipids as an emulsifying agent, the nurse checksfor any egg allergies before infusion. Other adverse reac-tions include fever, chills, chest tightness, dyspnea, tachy-cardia, headache, nausea, and vomiting.18 If such reactionsoccur, the infusion is stopped immediately and the reactionis reported to the physician and pharmacist. Before infu-sion, TPN solutions containing lipids are inspected for sep-aration of the lipid solution, also know as cracking andcoalescence. This loss of emulsion can be identified by yellow-brown marbling of the entire solution or a layering of oilat the surface. Such solutions are not safe for infusionand should be returned to the pharmacy for replacement.

Lipid solutions are isotonic and therefore help to reducethe osmolality of high dextrose concentrations when mixedtogether in a “3 in 1” admixture. Because of the expense ofthe equipment needed to compound lipids into the TPNsolution, some facilities opt to infuse lipids separately by IVpiggyback. Regardless of the method of delivery, weeklytriglyceride trends monitor tolerance. If serum triglyceridelevels exceed 500 mg/dL, lipids are often held until levelsreturn to normal.18 Use of a filter, no smaller than 1.2 µm,can reduce the incidence of particulates and air beingtransfused, thus reducing the risk of pulmonary embolism.There is no evidence, however, to suggest that these filtersreduce the risk of infection.19,20

Amino Acids. All tissues require protein to maintainstructure and facilitate wound healing. If protein intake isinadequate, the body becomes catabolic, seeking proteinfrom skeletal muscle and vital organs. In TPN, protein isprovided as a mixture of essential and nonessential crys-talline acids, which are available in concentrations rangingfrom 5% to 15%. Standard amino acid solutions containapproximately 50% amino acids and 50% nonessentialplus semiessential amino acids. For patients with renal dis-ease, there are solutions available with a higher concen-tration of essential amino acids. For patients with hepaticfailure or hypercatabolic conditions, there are formulaswith branched amino acids, which spare the breakdown ofother muscle proteins to use as energy, possibly reducingthe incidence of hepatic encephalopathy.

MicronutrientsVitamins, minerals, and trace elements are considered

micronutrients. Unfortunately, the U.S. RecommendedDietary Allowance requirements do not apply to par-enteral nutrition for multiple reasons. First, the liver and

gastrointestinal tract absorptive processes are bypassed,resulting in elimination of these micronutrients throughthe urine without their being utilized. Second, many dis-eases alter the gut’s ability to absorb fat-soluble vitaminsand vitamin B12. Finally, many nutrients adhere to the plas-tic tubing and IV solution bags or are destroyed by light andoxygen exposure (especially vitamin A) before reaching thebloodstream.3 With these factors in mind, standard aque-ous multivitamin preparations have been created. However,in hypermetabolic conditions, deficiencies that requireclose monitoring and potential supplementation can occur.Vitamin K is the only vitamin not included in the multi-vitamin preparation; it is provided by adding up to 10 mg/week of the vitamin to the TPN solution, unless contra-indicated by anticoagulation treatment.

Trace elements also come in a variety of commercial mix-tures but typically include chromium, copper, manganese,zinc, and selenium. Iron and iodine are not routinely addedto TPN solutions and may need to be supplemented inlong-term therapy.

Most electrolyte mixtures contain sodium, chloride,potassium, magnesium calcium, and phosphorus. Depend-ing on the patient’s underlying disease process and physicalassessment findings, specific electrolyte concentrations canbe adjusted daily in the TPN solution. If an electrolyte defi-ciency is detected after the TPN solution has already beenprepared or while infusing, additional IV supplements canbe given as a separate IV piggyback. Supplements andmedications should never be added to the TPN bag afterthe pharmacist has formulated it because this would breakthe sterility of the solution and may cause the solution toprecipitate.

MedicationsDuring the process of compounding the TPN solu-

tion, the pharmacist can add medications, many of whichare often necessitated by the TPN therapy itself. Forinstance, insulin is commonly added to the solutionsbecause of the increased incidence of hyperglycemia dur-ing TPN infusion. Also, heparin is often added to reducefibrin buildup along the catheter tip. Various medicationsare often added to treat underlying disease processes andtheir associated complications that necessitate the needfor TPN therapy.

PERIPHERAL PARENTERAL NUTRITIONPatients who need temporary nutritional support or whoneed to supplement the nutrient intake they are consum-ing orally or by tube feedings are optimal candidates forPPN. To decrease the incidence of phlebitis, an osmolar-ity of less than 800 mOsm/L is the goal to infuse PPN safelyby a peripheral vein.21 This osmolarity can be attained onlyby limiting the dextrose concentration and by increasingthe overall fluid volume and lipid concentration. Higherfluid volumes and reduced caloric/nutritional content limitPPN to short-term use, usually no more than 5 to 7 days.Therefore, goals of PPN are thought of in terms of pre-venting malnutrition, as opposed to correcting existingdeficits. PPN may be infused through a standard peripheralcannula or through long-term peripheral access devices.PPN can be reduced or discontinued once the patientbegins to tolerate oral or enteral feedings.

PPN requires good venous access, such as the basilicvein (see Fig. 40-3). The use of peripherally inserted cen-tral catheter lines increases patient comfort and improvesthe ability to provide nutrition through this access.

Complications of Parenteral NutritionComplications can be divided into four main categories:gastrointestinal, mechanical, metabolic, and infectious.

GASTROINTESTINAL COMPLICATIONSHepatic dysfunction may be seen in patients receivinglipid infusions; this is often related to the infusion amountand flow rate. Complications include hepatic steatosis(fatty liver), intrahepatic and extrahepatic cholestasis (sup-pression of bile flow), and cholelithiasis (formation of gall-stones). Although the exact mechanism for these hepaticdisorders is still not completely understood, it has beenobserved that cholestasis is less likely to occur if someform of enteral feeding is maintained.3

Gastrointestinal atrophy, and all of its associated compli-cations, may occur from disuse. If not contraindicated, oralor enteral feedings should be initiated as soon as possible.

MECHANICAL COMPLICATIONSMechanical complications include those associated withcentral venous catheterization insertion, such as trauma tothe vessel, pneumothorax, catheter occlusion, thrombo-sis, and venous air embolism. After insertion of a centralcatheter, a chest radiograph is the standard of care to con-firm correct placement. If there is a clinical suspicion ofcatheter tip migration or other potential complications,further diagnostic testing is indicated.

Trauma to vessels and pneumothorax are complicationsthat may warrant surgical intervention, insertion of a chesttube or tubes, or both. Catheter occlusion can simply be aresult of the catheter tip lodging against the vessel wall orbeing physiologically “pinched” between the clavicle andfirst rib. Occlusion can also occur from fibrin buildup(which accounts for 70% of occurrences of occlusion),blood or lipid deposition, drug precipitates, and catheterbreakage.22 Another type of occlusion, “withdrawal occlu-sion,” is an occlusion that allows infusion of a solution butprevents blood withdrawal. Although more research isneeded to determine optimal methods for catheter main-tenance and patency during parenteral nutrition infusions,routine flushing of catheters with diluted heparin (10 to100 units/mL in those without heparin sensitivities) is rec-commended.17

Thrombosis formation in the lumen of the vessel oftenresults from mechanical irritation (such as from traumaticcatheter insertion), a small lumen, an extended duration ofcatheter use, the catheter material, or malpositioning. Thereported rate of occurrence of subclavian thrombosis is2%, whereas the incidence of subclinical venous throm-bosis is near 50%.23 Therefore, nurses need to be awarethat patients may have a thrombosis and may be asympto-matic, yet complain of vague head and eye swelling on theaffected side.17 Vigilant assessments during parenteralnutrition administration are recommended. Treatmentincludes catheter removal, systemic anticoagulation, andthrombolytic therapy.



A venous air embolism is another serious complication,with a mortality rate of up to 50%.17 Any disruption of theclosed catheter system (usually during line connectionchanges, when hanging a new bag of TPN, or in an acci-dental tubing disconnection) can increase the risk for an air embolism. If such an incident occurs, the patientwill most likely experience acute, centrally located chestpain, dyspnea, and hypotension. Immediate nursing inter-ventions include clamping the tubing of the catheter oroccluding the catheter hub, attempting to aspirate airdirectly from the venous line, administering 100% oxy-gen, and placing the patient in steep Trendelenburg’sposition with the left lateral side down (because this posi-tion allows air to rise to the level of the right ventricle,away from the pulmonary vasculature).17,23 Prevention ofan air embolism can be facilitated by having the patientperform the Valsalva maneuver or simply hum audiblyduring line changes. In ventilator-dependent patients,positive intrathoracic pressure can be created by initiatingmechanical lung inflations or “breaths.” Finally, use ofsterile occlusive dressings (e.g., petroleum gauze) over thecatheter entrance site is an effective measure in prevent-ing air from entering the track after the catheter has beendiscontinued.17

METABOLIC COMPLICATIONSChecking each bag of parenteral nutrition solution for tran-scription accuracy, monitoring the IV pump for infusionaccuracy, and monitoring the patient’s response to therapyare all paramount in preventing serious metabolic compli-cations. It is important to understand that many metaboliccomplications stem from the patient’s underlying diseaseprocesses or from imprudent formula administration. Meta-bolic laboratory abnormalities, such as hyperglycemia andhypokalemia, can be treated by adjusting the formula’s con-centration of macronutrients, micronutrients, electrolytes,and insulin.

Virtually any metabolic disturbance can occur duringparenteral nutrition infusion. Glucose intolerance or hyper-glycemia, hypophosphatemia, hypokalemia, hypomagne-semia, and hypocalcemia are among the most commonmetabolic complications. Many of these metabolic distur-bances, coupled with fluid imbalances, may lead to refeed-ing syndrome.

HyperglycemiaHyperglycemia, or a blood sugar elevated over 220 mg/

dL, can occur if the pancreas does not respond to theincreased glucose load. Although it can be caused by eitherenteral or parenteral feedings, it is more commonly seen inpatients receiving parenteral nutrition. Even slightly ele-vated blood glucose levels can impair the function of lym-phocytes, leading to immunosuppression and increasedinfection risk. Elevated glucose concentrations have beenshown to reduce neutrophil chemotaxis and phagocytosisand may be an independent risk factor for short-terminfections.3 If the renal threshold for glucose reabsorptionis exceeded, osmotic diuresis results in subsequent dehy-dration and electrolyte imbalances. While compoundingthe TPN solution under sterile conditions, a pharmacistcan add insulin to the solution. Glycemic control can beachieved by increasing the amount of insulin in the TPN

solution, by maintaining a continuous insulin drip duringTPN administration, or by administering sliding-scaleinsulin subcutaneously at regular intervals. Once TPN is discontinued, insulin requirements will be notably less or nonexistent. When new TPN solution is tempora-rily unavailable, administration of 10% dextrose in water(D10W) is recommended to prevent rebound hypoglycemia.In addition, if a solution is “behind schedule,” it is notrecommended that the infusion rate be increased tomake up time; this may cause sudden metabolic fluctua-tions and fluid overload.

Refeeding SyndromeIn situations where a patient may be severely malnour-

ished, initiation of TPN may induce a phenomenon calledrefeeding syndrome. This is characterized by rapid changes inelectrolytes (phosphorus, potassium, magnesium, calcium),glucose, and volume status within hours to days of nutritionimplementation. Despite relatively normal serum phos-phorus levels, intracellular stores are markedly depleted inmalnourished catabolic patients. Glucose loads stimulateinsulin release, which in turn stimulates intracellular uptakeof phosphorus, glucose, and other electrolytes for anabolicprocesses. Severe hypophosphatemia (<1 mg/dL) can leadto neuromuscular, respiratory, and cardiac dysfunction.3Low serum levels of potassium, magnesium, and calciumcan precipitate cardiac arrhythmias. The increased intravas-cular fluid volumes, associated with parenteral nutrition inparticular, can strain the viscerally depleted heart and pos-sibly induce heart failure and myocardial damage.

Prevention and management of refeeding syndromeinclude correction of pre-existing glucose and electrolyteabnormalities before institution of nutritional therapy.Total volume and rate are titrated slowly to evaluate forfluid overload and potential cardiac decompensation. Accu-rate intake and output measurements and daily weights areof paramount importance because adequate parenteralnutrition often means giving 1.5 to 3 L of fluid per day inaddition to other therapies. If the patient has impaired car-diac or renal function, this could lead to fluid overload andcongestive heart failure; a progressive weight gain could bean early indicator of poor fluid tolerance.

INFECTIOUS COMPLICATIONSBoth the solution and the indwelling catheter are primesites for infection owing to the high glucose content. Anybreak in the system is a nidus for infection that can progressto a systemic infection if left unchecked. Therefore, thesolutions are prepared by a pharmacist under a laminarflow hood to ensure a particle-free, sterile environment.After initial preparation, the access hubs are often coveredwith tape as a reminder that no additional solutions ormedications are to be added.

At the bedside, the solution bag and tubing are changedaccording to institution policy, usually every 24 hours. Thecatheter insertion site is redressed per institution policy,usually every 24 to 72 hours, using either a sterile trans-parent or gauze dressing. Although transparent dressingsallow for easier observation of the catheter entrance site,these dressings have a tendency to trap more moisture andhence have a higher incidence of infection and sepsis thantraditional, sterile dry gauze dressings; however, this is still

feeding tolerance are obtained through abdominal exami-nations, which assess bowel sounds and changes in abdom-inal girth. Volume and frequency of both urine and stoolare monitored and recorded.

The nurse must also monitor for clinical signs ofdehydration (thirst, dry mucous membranes, tachycar-dia, and poor skin turgor), and fluid excess (peripheraledema and adventitious lung sounds). Early detectionand subsequent interventions may prevent the occur-rence of excessive fluid shifts and cardiac compromise.This is of special concern if the patient is severely mal-nourished, which may precipitate refeeding syndromeand other untoward complications. Meticulous feedingtube and IV catheter care is critical to preventing localand systemic forms of infection.

Care also includes providing information and emo-tional support to the patient and family. Examples includeexplaining the procedure, what to expect, risks, and ex-pected outcomes (Box 40-4). Guidelines for dischargeplanning are given in Box 40-5.

clinical applicability challenges

Self-Challenge: Critical Thinking1. An elderly man is status post-right cerebral vascular acci-

dent, resulting in left hemiparesis and severe dysphagia.Despite daily work with a speech and swallowing specialist,oral feeding is contraindicated because of high risk for aspi-ration. His wife gives consent for surgical placement of a per-cutaneous endoscopic gastrostomy (PEG) tube for long-termmanagement of nutrition and hydration. Explore why thistube placement was chosen.a. Is this an appropriate intervention for this patient? Why

or why not?b. What are the alternatives?

Study Questions1. The most accurate method of determining initial nasogastric

feeding tube placement isa. auscultating for air over the gastric region.b. aspirating secretions and checking the pH.c. abdominal radiography.d. both a and b.

2. Immediately after an open cholecystectomy, a patient is startedon enteral tube feedings at goal rate. Twelve hours aftersurgery, the patient has had four episodes of diarrhea, approx-imately 475 mL. Bowel sounds are present. The most appro-priate and initial nursing action would be toa. request that the patient be changed to parenteral

nutrition.b. request that the patient be changed to maintenance

intravenous IV fluids only.c. reduce the rate of the enteral feeding infusion.d. send stool for Clostridium difficile cultures.

3. A patient has a duodenal feeding tube placed endoscopicallypast the pylorus. The nurse giving you the report tells youthat the patient is receiving enteral nutrition at goal rateof infusion of 60 mL/hour; however, he is concerned thatthe residual 1 hour ago was 125 mL. An abdominal film

under investigation.3 At the time of the dressing change,the site should be examined for signs of leakage, erythema,edema, and inflammation. The skin must be cleansed wellwith an antibacterial solution to remove pathogenic organ-isms. Chlorhexidine solution has been shown to be a moreeffective local antiseptic than iodophor or alcohol.24 Thepresence of a tracheostomy or other open draining woundsnear the IV insertion site requires special precautions toprevent site contamination.

Potential for infection can be minimized by meticulouscatheter care. In critically ill patients, catheter-related infec-tions range from local inflammation to systemic blood-stream infection and sepsis. Systemic catheter-relatedinfections are associated with a 35% mortality rate, andhospital stays are reportedly longer and more expensive asa result of complications and associated treatment.3,25,26 Iffever, rigors, or chills coincide with parenteral infusion,catheter-related sepsis should be suspected; slowing orstopping the infusion may cause defervescence.3 Treatmentof an infection may involve local topical antibiotics, sys-temic antibiotics, and, in many cases, catheter removal. Ifcatheter sepsis is suspected, the catheter tip is usually cul-tured to identify the offending organism for appropriateantibiotic coverage.

Terminating Parenteral NutritionTapering or cycling (bedtime) TPN is often given inthose patients who are able safely to resume (and toler-ate) oral or enteral nutrition. In such instances, a caloriecount is essential to ascertain that the patient’s nutri-tional needs are being met. Before discontinuation ofparenteral nutrition, the infusion rate is decreased byhalf for 30 to 60 minutes to allow for a plasma glucoseresponse and prevention of rebound hypoglycemia.27

Checking blood sugars within a 30- to 60-minute win-dow after discontinuation helps the nurse identify andmanage immediate glucose abnormalities.

In situations where poor prognosis does not warrantaggressive nutritional support, emotional and ethical dilem-mas may surface for many nurses because feeding and hydra-tion have long been basic tenets of nursing care. Althoughmany institutions may have protocols in place regardingparenteral nutrition, treatment decisions and plan of careshould be discussed on an individual basis; frequent,ongoing discussions between the patient, family, and thehealth care team are imperative to providing the bestpossible care to each patient.

ROLE OF THE NURSEIN NUTRITIONAL SUPPORT

Nurses are responsible for obtaining initial “dry weight”and weekly weight measurements, vital signs, intake andoutput measurements, and laboratory data, and for pro-viding enteral tube and IV catheter care throughout theduration of nutrition support therapies. Many complica-tions, whether from enteral or parenteral nutrition, can beprevented by vigilant observation and care. If the patient isawake and alert, the patient’s subjective assessment of tol-erance can be very informative. More objective signs of



confirms correct placement. The most appropriate nursingaction is toa. hold tube feedings for 2 hours and restart at a lower rate.b. resume tube feedings as ordered and monitor for nausea/

vomiting; residuals postpyloric may be misleading.c. discontinue enteral feedings and request parenteral

nutrition be initiated.d. hold tube feedings for 4 hours and restart after diluting

with water.

4. Which of the following macronutrients in parenteral nutri-tion may need to be increased in a patient who has large,nonhealing wounds?a. Carbohydratesb. Lipidsc. Trace elementsd. Protein

REFERENCES1. Souba WW: Nutritional support. N Engl J Med 336(1):41–48,

19972. Braunschweig C, Gomez S, Sheean PM: Impact of declines in

nutritional status outcomes in adult patients hospitalized for morethan 7 days. J Am Diet Assoc 100(11):1316–1324, 2000

3. Braunwald E, Fauci AS, Kasper DL, et al: Enteral and parenteralnutrition therapy. In Harrison TR (ed): Principles of Internal Med-icine (15th Ed), pp. 470–478. New York, McGraw-Hill, 2001

4. Marian MJ, Allen P: Nutrition support for patients in long-term acutecare and subacute care facilities. AACN Clin Issues 9(3):427–440,1998

5. Cerra FB, Blackburn GL, Jeejeebhoy K, et al: Applied nutrition inICU patients: A consensus statement of the American College ofChest Physicians. Chest 111(3):769–778, 1997

6. Guenter P, Jones S, Ericson M: Enteral nutrition therapy. NursClin North Am 32(4):651–668, 1997

7. Bliss DZ, Lehmann S: Tube feeding administration tips. RN 62(8):29–32, 1999

8. Kirby DF, Delegge MH: American Gastroenterological Associationmedical position statement: Guidelines for the use of enteral nutri-tion. Gastroenterology 108(4):1280–1301, 1995

9. Stone SJ, Pickett JD, Jesurum JT: Bedside placement of postpyloricfeeding tubes. AACN Clin Issues 11(4):517–530, 2000

10. Grant MC, Martin S: Delivery of enteral nutrition. AACN ClinIssues 11(4):507–516, 2000

11. Bowers S: All about tubes: Your guide to enteral feeding devices.Nursing 2000 30(12):41–48, 2000

12. Lord LM: Enteral access devices. Nurs Clin North Am 32(4):685–704, 1997

13. Loan T, Magnuson B, Williams S: Debunking six myths aboutenteral feeding. Nursing 98 28(8):43–49, 1998

box 40-4Living With Nutritional Support

General Care: Enteral Nutrition■ Administer enteral formulas as prescribed.■ Know potential complications and appropriate treatments.■ Avoid activities that may result in high impact or stress

at the insertion site and report any activity that mayhave damaged the enteral access site.

■ Return to previous activities (e.g., work, leisure, sexualactivity) after obtaining physician consent.

General Care: Parenteral Nutrition■ Administer parenteral formulas as prescribed.■ Monitor blood sugars closely to help determine toler-

ance of parenteral solutions.■ Know the potential complications and appropriate

treatments.■ Avoid activities that may result in high impact or stress

at the insertion site and report any activity that mayhave damaged the parenteral access site.

■ Return to previous activities (e.g., work, leisure, sexualactivity) after obtaining physician consent.

Signs of Infections■ Understand the rationale for aseptic technique.■ Notify the nurse of symptoms of fever, localized

warmth, redness, pain, or drainage at the feedingtube or intravenous insertion site.

Medications■ Follow instructions regarding medications.■ Know the names of medications and the dose, fre-

quency of administration, side effects, and use of eachmedication.

■ Know the proper technique of administering medica-tions through the feeding tube and proper flushingtechnique.

■ Never add medications to TPN solutions—they shouldbe added by the supplier because of risk of contamina-tion or precipitation of the formula.

Safety Measures■ Inform other health care providers of either enteral or

parenteral access devices and notify them of any med-ications that the patient may be taking.

Follow-up Care■ Report any problems to the home care nurse.■ Adhere to schedule for follow-up visits with patient’s

physician or clinic.

box 40-5 Nutritional Therapy

■ Assess patient/caregiver ability to deliver home nutri-tional therapy, including physical and cognitive abilities.

■ Identify health care team members who will be respon-sible for the management of home therapy.

■ Assess patient’s home environment for safety.■ Evaluate support system available in home.■ Identify an in-home caretaker who is willing and able to

learn and carry out the home care regimen. If thepatient does not have a caretaker at home and thereare concerns about patient’s ability to become inde-pendent, reevaluate discharge plan.

■ Ensure that patient/caregiver learning includes deter-mining procedures and risks, picking up patient andequipment problems early, troubleshooting, and fol-lowing up with the health care provider.

■ Refer to and communicate with home care services.■ Provide written instructions for patient.■ If possible, do not change the amount or rate of nutri-

tion support on the day of discharge to home.

14. Weinstein DS, Furman J: Enteral formulas. Nurs Clin North Am32(4):669–683, 1997

15. DeWitt RC, Kudsk KA: Enteral nutrition. Gastroenterol ClinNorth Am 7(2):371–386, 1998

16. Morrisson SG: Feeding the elderly population. Nurs Clin NorthAm 32(4):791–812, 1997

17. Worthington P, Gilbert KA, Wagner BA: Parenteral nutrition forthe acutely ill. AACN Clin Issues 11(4):559–579, 2000

18. Heimburger DC, Weinster RL: Handbook of Clinical Nutrition(3rd Ed). St. Louis, Mosby, 1997

19. A.S.P.E.N. Board of Directors: Safe practices for nutrition formu-lations. JPEN J Parenter Enteral Nutr 22:49–66, 1998

20. U.S. Food and Drug Administration: Safety Alert: Hazards of pre-cipitation associated with parenteral nutrition. Am J Hosp Pharm51:1427–1442, 1994

21. Semrad CE: Parenteral nutrition. Clin Perspect Gastroenterol 3(6):307–313, 2000

22. Wickham RS: Advances in venous access devices and nursing man-agement strategies. Nurs Clin North Am 25:345–364, 1990

23. Hinke DH, Zandt-Stastny DA, Goodman LR, et al: Pinch-off sign:A complication of implantable subclavian access devices. Radiology177:353–356, 1990

24. Maki DG, Ringer M, Alvarado CJ: Prospective randomized trial ofpovidone-iodine, alcohol, and chlorhexidine for prevention of infec-tion associated with central venous and arterial catheters. Lancet338:339, 1991

25. Krzywda EA, Andris DA, Edminston CE: Catheter infections: Diag-nosis, treatment, and prevention. Nutr Clin Pract 14:178–190, 1999

26. U.S. Department of Health and Human Services, Public HealthService, Centers for Disease Control and Prevention: Guideline forprevention of intravascular device-related infections. Am J InfectControl 24:262–293, 1996

27. Krzydwa EA, Andris DA, Whipple JA, et al: Glucose response toabrupt initiation and discontinuation of total parenteral nutrition.JPEN J Parenter Enteral Nutr 17:64–67, 1991

OTHER SELECTED READINGAdams GF, Guest DP, Ciraulo DL, et al: Maximizing tolerance of

enteral nutrition in severely injured trauma patients: A comparisonof enteral feedings by means of percutaneous endoscopic gastros-tomy versus percutaneous endoscopic gastrojejunostomy. J Trauma48(3):459–465, 2000

American Society for Gastrointestinal Endoscopy: The role of PEG/PEJin enteral feeding. Gastrointest Endosc 48(6):699–701, 1998

Braunschweig CL, Levy P, Sheean PM, et al: Enteral compared with par-enteral nutrition: A meta analysis. Am J Clin Nutr 74:534–542, 2001

Dimick J, Swoboda S, Talamini M, et al: Risk of colonization for centralvenous catheters: Catheters for total parenteral nutrition versus othercatheters. Am J of Crit Care 12(4):328–335, 2003

Dranoff JA, Angood PJ, Topazian M: Transnasal endoscopy for enteralfeeding tube placement in critically ill patients. Am J Gastroenterol94(10):2902–2904, 1999

Evans-Stoner N: Guidelines for care of the patient on home nutritionsupport: An appendix. Nurs Clin North Am 32(4):769–775, 1997

Garrett K, Tsuruta K, Walker S, et al: Managing nausea and vomiting:Current strategies. Criti Care Nurse 23(1):31–52, 2003

Hammond K: Physical assessment: A nutritional assessment. Nurs ClinNorth Am 32(4):779–790, 1997

Horn D, Chaboyer W: Gastric feeding in critically ill children: A ran-domized controlled trial. Am J of Crit Care 12(5):461–468, 2003

Karch AM: 2002 Lippincott’s Nursing Drug Guide. Philadelphia,Lippincott Williams & Wilkins, 2002

Kohn-Keeth C: How to keep feeding tubes flowing freely: How to clearthe way if clogging occurs. Nursing 2000 30(3):58–59, 2000

Kudsk KA, Croce MA, Fabian TC, et al: Enteral versus parenteral feed-ing: Effects on septic morbidity after blunt and penetrating abdominaltrauma. Ann Surg 215:503–511, 1992

Lacy CF, Armstrong LL, Golman MP, et al: Drug Information Hand-book (9th Ed). Hudson, OH, Lexi-Comp, 2001

Lenart S, Polissar NL: Comparison of 2 methods for postpyloric place-ment of enteral feeding tubes. Am J of Crit Care 12(4):357–360,2003

Loan T, Kearney P, Magnuson B, et al: Enteral feeding in the homeenvironment. Home Healthcare Nurse 15(8):531–538, 1997

Marino PL: The ICU Book (2nd Ed). Baltimore, Williams and Wilkins,1998

Marshall AP, West SH: Gastric tonometry and enteral nutition: A pos-sible conflict in critical care nursing practice. Am J of Crit Care12(4):349–356, 2003

Metheny NM: Fluid and Electrolyte Balance: Nursing Considerations(4th Ed). Philadelphia, Lippincott Williams & Wilkins, 2000

Olsen J: Clinical Pharmacology Made Ridiculously Simple (2nd Ed).Miami, Medmaster, 2001

Parrish CR: Protocols for practice: Applying research at the bedside. CritCare Nurse 19(1):91–94, 1999

Powers J, Chance R, Bortenschlager L, et al: Bedside placement of small-bowel feeding tubes in the intensive care unit. Crit Care Nurse23(1):16–24, 2003

Medical Economics Staff: PDR: Physicians Desk Reference (56th Ed).Montvale, NJ, Medical Economics, 2002

Medical Economics Staff: Physician’s Desk Reference for Nonprescrip-tion Drugs and Dietary Supplements (22nd Ed). Montvale, NJ, Med-ical Economics, 2001

Reddy P, Malone M: Cost and outcome analysis of home parenteral andenteral nutrition. JPEN J Parenter Enteral Nutr 22(5):302–310, 1998

Roberts SR, Kennerly DA, Keane D, George C: Nutrition support in theintensive care unit: Adequacy, timeliness, and outcomes. Crit CareNurse 23(6):49–57, 2003

Schiff L (ed): Enhanced enteral feeding formulas. RN 63(9):77–79, 2000


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